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Trent P Munro1, Sunjong Kwon2,
Bruce Schnapp2, Daniel St Johnston1. 1)
The Gurdon Institute, University of Cambridge, Cambridge, United
Kingdom; 2) Department of Cell and Developmental Biology, Oregon
Health Sciences University, 3181 S.W. Sam Jackson Park Road
Portland, Oregon 97201-3098, USA.
ZBP (zipcode binding protein) has previously been implicated in the
localisation of
β-actin mRNA to the motile edge of fibroblasts. This localisation
allows for the rapid and regulated translation of actin protein at
the migratory edge of the cell. We have analysed the role of the
Drosophila orthologue of ZBP, known as IMP, and have shown egg
chambers mutant for IMP have severe border cell migration defects.
Furthermore IMP mutant embryos show a number of other phenotypes
consistent with defects in cell migration.
Border cells are a specialised group of 6-8 follicle cells that
delaminate as a cluster from the anterior of the egg chamber and
migrate directionally between the nurse cells toward the oocyte. The
events that underpin this process are similar to those that occur in
metastatic neoplasms and therefore border cell migration is an
attractive model system in which to study cell migration.
During migration, dynamic, actin-rich protrusions extend from the
cells at the leading and trailing edge of the cluster. In IMP
mutants the border cell cluster is clearly specified however the
actin-rich protrusions that precede migration fail to form and the
cluster remains at the anterior. We show that there is a pool of
β-actin mRNA in these pre-migratory protrusions and that RNA from
Actin 42A is specifically found in these cells. In addition RNA
binding experiments show that the 3’UTR from Actin 42A is
specifically recognised by IMP. We propose that IMP provides a key
mechanism for the control of cell migration via its regulation of
both the localisation and translation of
β-actin mRNA. |
